Literature DB >> 22375061

The IplA Ca2+ channel of Dictyostelium discoideum is necessary for chemotaxis mediated through Ca2+, but not through cAMP, and has a fundamental role in natural aggregation.

Daniel F Lusche1, Deborah Wessels, Amanda Scherer, Karla Daniels, Spencer Kuhl, David R Soll.   

Abstract

During aggregation of Dictyostelium discoideum, nondissipating, symmetrical, outwardly moving waves of cAMP direct cells towards aggregation centers. It has been assumed that the spatial and temporal characteristics of the front and back of each cAMP wave regulate both chemokinesis and chemotaxis. However, during the period preceding aggregation, cells acquire not only the capacity to chemotax in a spatial gradient of cAMP, but also in a spatial gradient of Ca(2+). The null mutant of the putative IplA Ca(2+) channel gene, iplA(-), undergoes normal chemotaxis in spatial gradients of cAMP and normal chemokinetic responses to increasing temporal gradients of cAMP, both generated in vitro. However, iplA(-) cells lose the capacity to undergo chemotaxis in response to a spatial gradient of Ca(2+), suggesting that IplA is either the Ca(2+) chemotaxis receptor or an essential component of the Ca(2+) chemotaxis regulatory pathway. In response to natural chemotactic waves generated by wild-type cells, the chemokinetic response of iplA(-) cells to the temporal dynamics of the cAMP wave is intact, but the capacity to reorient in the direction of the aggregation center at the onset of each wave is lost. These results suggest that transient Ca(2+) gradients formed between cells at the onset of each natural cAMP wave augment reorientation towards the aggregation center. If this hypothesis proves correct, it will provide a more complex contextual framework for interpreting D. discoideum chemotaxis.

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Year:  2012        PMID: 22375061      PMCID: PMC3346828          DOI: 10.1242/jcs.098301

Source DB:  PubMed          Journal:  J Cell Sci        ISSN: 0021-9533            Impact factor:   5.285


  87 in total

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10.  Overexpressing TPTE2 (TPIP), a homolog of the human tumor suppressor gene PTEN, rescues the abnormal phenotype of the PTEN-/- mutant.

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  10 in total

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